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The mutation causes an approximately 40% reduction in the formation of amyloidogenic peptides in vitro.
The mutation causes an ion channel protein on the surface of brain cells to be overly active, changing how the nerve cells function and ultimately how the brain develops and works.
Therefore, data above altogether indicate that the atjmj4 mutation causes an early flowering independently of FLC expression.
The finding that the H379A mutation causes an approximately 50% reduction in Hhat PAT activity agrees with our previous report [11].
Lack of germline proliferation in C. elegans, either by laser ablation of the germ cell precursors or by mutation, causes an increase in lifespan [8], [9].
This non-synonymous mutation causes an Arg206His amino acid substitution within the GS (glycine-serine rich) domain of the ACVR1 protein, and has been confirmed by our further work and also by others [6], [7].
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In Marfan syndrome a genetic mutation causes a defect in the production of fibrillin, a protein found in connective tissue.
We suspect that the N159V mutation causes a relatively large structural perturbation in the substrate binding pockets.
Among them, one mutation causes a 13 bp deletion leading to a frame shifting of the coding sequence and appearance of a premature stop codon (Fig. 4C).
This mutation causes a small, nonfunctional form of the protein chorein to be produced.
The mutation causes a frame shift and results in a premature stop codon.
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